Gastroduodenal Disorders
  • Source: Gastroenterology, Rome Foundation/V (Accepted Date: 20 January 2026)
  • Topic: Classification, Diagnosis, and Management of Gastroduodenal Disorders (DGBI)
  • Author(s): Hans Törnblom, Florencia Carbone, William L. Hasler, André Smout, Hidekazu Suzuki, Jan Tack, Nicholas J. Talley, Vincenzo Stanghellini
1. Overview and Classification

Symptoms attributable to the gastroduodenal area are classified into five categories:

  • Functional Dyspepsia (FD) → Postprandial Distress Syndrome (PDS) + Epigastric Pain Syndrome (EPS)
  • Nausea and Vomiting Disorders → Chronic Nausea/Vomiting Syndrome (CNVS), Cyclic Vomiting Syndrome (CVS), Cannabinoid Hyperemesis Syndrome (CHS)
  • Excessive Belching Disorders → Gastric + Supragastric belching
  • Inability to Belch Syndrome (new category)
  • Rumination Syndrome
  • RFGES prevalence: 10.6% of general population has gastroduodenal DGBI
2. Functional Dyspepsia: Definition and Epidemiology
2.1 Definition
  • Dyspeptic symptoms: bothersome postprandial fullness, early satiation, epigastric pain, epigastric burning
  • Secondary dyspepsia: structural/systemic/metabolic disease identified
  • FD: no explanation found after diagnostic procedures
  • PDS/EPS specifiers used based on symptom profile
2.2 Epidemiology
  • RFGES prevalence: 7.2% (95% CI 7.0–7.4) for FD symptoms
3. Functional Dyspepsia: Diagnostic Criteria
3.1 General FD Criteria (B1)

Must fulfill both:

1. One or more: bothersome postprandial fullness, early satiation, epigastric pain, epigastric burning

2. No evidence of structural/systemic/metabolic disease explaining symptoms

  • Criteria: last 3 months, onset ≥6 months before diagnosis
3.2 Postprandial Distress Syndrome (B1a)

Required (≥2 days/week):

  • Bothersome postprandial fullness (impacts usual activities)
  • OR bothersome early satiation (prevents finishing regular-sized meal)

Associated features:

  • Other food-induced symptoms allowed: postprandial epigastric pain/burning, nausea, bloating, excessive belching
  • Predominant nausea/persisting vomiting → exclude PDS, consider CNVS/gastroparesis
  • Heartburn not a gastroduodenal symptom but may coexist
  • Postprandial = symptoms within 2 hours of meal intake
3.3 Epigastric Pain Syndrome (B1b)

Required (≥1 day/week):

  • Bothersome epigastric pain OR epigastric burning (impacts usual activities)
  • Can be postprandial or meal-independent
  • PDS criteria not fulfilled
  • Predominant nausea/vomiting → exclude EPS

Provisional subcategories:

  • Meal-related EPS: epigastric pain/burning worsens after meals in ≥50% of times
  • Meal-unrelated EPS: worsening in <50%
4. Functional Dyspepsia: Pathophysiology
4.1 Disordered Motility
  • Impaired gastric accommodation (IGA): found in up to 40% of FD patients → leads to altered meal distribution toward distal stomach
  • IGA associated with: early satiation, postprandial fullness, unintentional weight loss
  • Delayed gastric emptying: ~30% of FD patients → associated with more severe upper GI symptoms (especially postprandial fullness, nausea, vomiting)
  • Visceral hypersensitivity: up to 30% of FD patients → initially correlated to EPS, also associated with meal-related symptom severity
  • Chemical stimuli (acid, nutrients, lipids) impact visceral sensitivity
  • Altered gut peptide release affects gastroduodenal motility
4.2 Duodenal Alterations
  • Barrier dysfunction: linked to increased mucosal permeability and immune activation
  • Meta-analysis: higher duodenal eosinophils and mast cells in FD, more pronounced in post-infection FD
  • Budesonide treatment → reduction in duodenal eosinophils correlates with symptom reduction (postprandial fullness, early satiation)
  • PPI use in FD → decreased eosinophil/mast cell counts, improved barrier function, decreased symptom severity
4.3 Altered Microbiome
  • Duodenal biopsies show differences in bacterial phyla: Firmicutes, Fusobacteriota, Patescibacteria vs controls
  • Overlapping IBS and PPI use are potential confounders
4.4 Bile Salt Composition
  • Ratio of fasting primary:secondary bile salts decreased in FD vs healthy subjects
  • Bile salt concentration correlates with impaired duodenal permeability
  • Vitamin D receptor (bile acid sensor) expression increased in FD
  • Inverse correlation between GE rate and duodenal bile salts
4.5 Adverse Reactions to Nutrients
  • Most FD patients report food-triggered/aggravated symptoms
  • FODMAP elimination: beneficial effect on symptoms + improved intraepithelial flux across duodenal mucosa
  • Confocal laser endomicroscopy: food induces acute immune reactions (eosinophils) in duodenal mucosa
  • 6-food elimination diet: beneficial effect in FD
4.6 Neuronal Dysfunction
  • Low-grade inflammation linked to neuro-immune dysregulation
  • Mast cells show closer proximity to duodenal submucosal nerve endings in FD → correlates with GI symptom numbers and epigastric pain
  • Eosinophil/mast cell counts in submucous plexus correlate with submucosal neuronal structural/functional damage
4.7 Stress
  • Dysregulated duodenal hypothalamic-pituitary-adrenal (HPA) axis signaling in FD
4.8 Altered Brain Processing
  • Clear associations between psychological comorbidities and FD
  • Symptom severity and weight loss associated with psychosocial factors and somatization
  • History of abuse → alterations in gastric sensorimotor function + PDS symptoms
  • FD patients perceive life events as more stressful
  • Bidirectional interaction between FD symptoms and psychological comorbidities over time
4.9 Genetics
  • FD has weak heritability
  • Meta-analysis: no association with specific single nucleotide polymorphisms
  • Inconsistencies between candidate gene studies
4.10 Pathogenic Micro-organisms
  • Acute gastroenteritis (bacteria, viruses, parasites) → increased FD risk
  • Post-infection onset associated with weight loss and early satiety
  • Meta-analysis: increased duodenal eosinophils in post-infection FD vs controls
4.11 Helicobacter pylori Infection
  • H. pylori gastritis with characteristic findings (Kyoto classification) → considered organic disease
  • Eradication therapy effective in ~30% of FD patients with NNT = 15
  • If symptom remission persists ≥6 months after eradication → diagnosed as H. pylori-associated dyspepsia (HpD)
5. Functional Dyspepsia: Clinical Evaluation
5.1 Diagnostic Algorithm
  • Management guided by patient history
  • In absence of alarm features: discontinue unnecessary drugs/supplements causing dyspepsia before further testing
  • H. pylori status must be determined in every dyspeptic patient
5.2 Testing Recommendations
  • Routine laboratory testing (including celiac serology): not recommended due to low diagnostic yield
  • No international consensus on routine duodenal biopsies
  • Standard clinical practice: uninvestigated dyspepsia managed without upper endoscopy if no alarm features
  • Upper endoscopy mandatory for: alarm features, clinical trial, mechanistic trial
  • No evidence supporting routine imaging in FD diagnostic workup
  • Additional testing considered for: abnormal clinical examination, failed treatment (case-by-case)
  • Motility studies in routine FD diagnosis: not recommended
6. Functional Dyspepsia: Treatment
6.1 Dietary and Lifestyle Advice
  • Evidence for diet as therapeutic strategy: low
  • Reasonable advice: frequent small-size meals, avoid high-fat foods
6.2 H. pylori Eradication
  • Consider H. pylori as cause if eradication → sustained symptom benefit
6.3 Proton Pump Inhibitors (PPI)
  • First-line for FD patients symptomatic after H. pylori eradication or H. pylori-negative
  • Standard once-daily dose for 4–8 weeks, discontinue if insufficient improvement
  • No dose escalation strategy recommended
  • NNT = 11 for global symptom reduction
  • Evidence limited in FD subgroups, no data in EPS-PDS overlap group
  • PPI may be less effective for PDS symptoms
6.4 Histamine-2 Receptor Blockers (H2RA)
  • NNT = 7, but low study quality, inclusion of GERD patients likely
  • Most guidelines suggest PPI over H2RA as first-line (except NICE guidelines: both options)
6.5 Prokinetics
  • Heterogeneous class: anti-emetic properties (D2 antagonists) or prokinetic activity (5-HT4 agonists, cholinesterase inhibitors)
  • Meta-analysis
6.5 Prokinetics (continued)
  • Meta-analysis demonstrated significant effect in reducing dyspeptic symptoms with NNT = 12 (excluding cisapride)
  • 5-HT4 agonists: tegaserod showed benefit in female FD patients
  • Itopride (D2 antagonist + cholinesterase inhibitor): significantly more responders based on global efficacy measure and Leuven postprandial distress scale in PDS-EPS overlap (Rome III)
  • Acotiamide (cholinesterase inhibitor, M1/M2 muscarinic antagonist): enhances gastric accommodation and GE rate, well-tolerated, most effective for PDS
6.6 Neuromodulators
  • Centrally acting neuromodulators effective for FD with NNT = 6
  • Beneficial effect limited to tricyclic antidepressants (TCA) and antipsychotics (e.g., levosulidazole with prokinetic activity)
  • Longest therapy duration: 12 weeks → long-term efficacy unknown
  • Both adverse event number and withdrawal rates higher with psychotropic drugs
  • Amitriptyline effects on pain potentially more useful in EPS
  • Two SSRI studies in FD: negative
  • Mirtazapine: improves early satiation scores, nutrient tolerance, associated with significant weight loss recovery, QoL improvement, reduced GI-specific anxiety
  • Tandospirone citrate (5-HT1A agonist): improves abdominal symptom score, overall dyspeptic severity, individual symptoms (postprandial fullness, early satiation, upper abdominal bloating); increases gastric accommodation and delays GE of liquids
  • Meta-analysis: FD patients treated with 5-HT4 or 5-HT1A agonists show significantly greater symptom improvement vs placebo
6.7 Herbal Therapies
  • STW 5 and STW 5-II: superior to placebo in FD treatment
  • Peppermint oil + caraway oil combination: superior to placebo
  • Rikkunshito (Japanese herbal KAMPO preparation): efficacy and safety in FD
  • Zhi Zhu KuangZhong: symptom-reducing effect in PDS
  • Biling Weitong granules: superior to placebo in reducing epigastric pain severity in EPS
6.8 Probiotics
  • Lactobacillus gasseri OLL2716 (LG21): daily intake for 3 months → higher improvement rates for PDS symptoms (not EPS)
  • Bacillus subtilis + coagulans strains: effective for key individual FD symptoms
  • Review summarizes probiotic effects in FD
6.9 Psychological and Behavioral Therapies
  • At least 4 studies on CBT: all showed positive short-term effects on FD symptoms
  • One study: sustained efficacy after 6 months follow-up
  • Positive results of hypnotherapy in FD reported in one small RCT
6.10 Acupuncture
  • Meta-analyses of numerous low-quality RCTs suggest manual and electric acupuncture effective in FD treatment
  • Major concerns: selection bias, performance bias, reporting bias, attrition bias
6.11 Proposed Management Algorithm for PDS
  • Dietary/lifestyle advice precedes pharmacotherapy
  • First-line: PPI, first-line prokinetic agents, or herbal preparations (STW 5, STW 5-II, rikkunshito, peppermint oil/caraway oil, or better-studied Chinese herbal medicines) → choice depends on clinical experience and agent availability
  • Insufficient response: endoscopy and other tests recommended if not yet performed
  • Second-line: neuromodulators
  • Refractory early satiation → consider 5-HT1A agonist (tandospirone or buspirone)
  • Weight loss → mirtazapine option
  • TCA may show efficacy for postprandial fullness
  • Non-responders: consider GE test → if significant delay, second-line prokinetic agents (prucalopride, levo-sulpiride) → classified as "PDS with delayed GE"
  • Gastroparesis term reserved for predominant nausea or recurrent vomiting
6.12 Proposed Management Algorithm for EPS
  • Dietary/lifestyle advice precedes pharmacotherapy
  • First-line: PPI or herbal preparations with established efficacy/safety profile
  • Insufficient response: endoscopy and other tests recommended if not yet performed
  • Second-line: neuromodulators, specifically TCA
  • Both EPS and PDS: nutritional support recommended for refractory symptoms with weight loss or feeding restrictions
7. Nausea and Vomiting Disorders: Definition
7.1 Core Concepts
  • Nausea: unpleasant sensation of impending need to vomit
  • Vomiting: forceful oral expulsion of GI contents from mouth (distinguished from regurgitation = effortless passage)
  • Diagnostic approach to chronic/recurrent nausea/vomiting: see Figure 5
8. Nausea and Vomiting Disorders: Diagnostic Criteria
8.1 Chronic Nausea and Vomiting Syndrome (CNVS) - B2a

Must include ALL:

1. Bothersome nausea ≥2 days/week with or without ≥1 vomiting episode/week

2. Exclude: self-induced vomiting, eating disorders, regurgitation, rumination as cause

3. No evidence of structural/systematic/metabolic disease on routine investigations

4. Symptoms predominantly due to PDS → exclude diagnosis

5. Predominant nausea/persistent vomiting with delayed GE → prompt gastroparesis diagnosis

  • Criteria: last 3 months, onset ≥6 months before diagnosis
8.2 Cyclic Vomiting Syndrome (CVS) - B2b

Must include ALL:

1. Stereotypical repetitive vomiting episodes regarding onset (acute) and duration (up to 10 days)

2. ≥3 discrete episodes in prior year, ≥2 episodes in past 6 months, occurring ≥1 week apart

3. Milder symptoms (nausea, isolated vomiting) can be present between cycles

  • Supportive: history or family history of migraine headaches
8.3 Cannabinoid Hyperemesis Syndrome (CHS) - B2c

Must include ALL:

1. Stereotypical episodic vomiting resembling CVS in onset, duration, frequency

2. Presentation after prolonged (≥1 year) and excessive (≥4 days/week and/or ≥15 doses/week) cannabis use

3. Relief of vomiting episodes by sustained (≥6 months or 3 typical emetic cycles) cessation of cannabis use

  • Supportive: may be associated with pathologic bathing behavior (prolonged hot baths/showers)
9. Nausea and Vomiting Disorders: Justification for Criteria Changes
9.1 CNVS Updates
  • Symptom frequency changed to >2 nausea days weekly with or without >1 weekly vomiting episodes
  • Question PDS symptoms when evaluating for CNVS → PDS diagnosis if dominant
  • Delayed GE with CNVS symptoms → prompt gastroparesis diagnosis
9.2 CVS Updates
  • Minor changes: acknowledge some patients experience minor vomiting during interepisodic phases
9.3 CHS Updates
  • Quantified cannabis-use profiles and durations of abstinence for diagnosis
10. Nausea and Vomiting Disorders: Epidemiology
10.1 CNVS Epidemiology
  • Unexplained vomiting ≥once monthly: 2–3% of individuals
  • Nausea ≥weekly: 3%
  • RFGES: nausea without vomiting reported by 1.9% of responders (unpublished) → more common in women and those <40 years
  • Rome IV survey: CNVS prevalence 0.8–1.2%
  • Associated with IBS (41%) and FD (55%)
  • Reduced quality of life
10.2 CVS Epidemiology
  • Rome IV survey: prevalence 1.4% → greater in US vs Canada/UK
  • Japan prevalence lower: 0.05 cases/1,000 population
  • Mean age of onset: 32 years
  • More common in women
10.3 CHS Epidemiology
  • Debated whether CHS is CVS subtype or distinct entity
  • Advocacy for distinct diagnosis: pathophysiology and treatment differ from CVS
  • Up to 80% of CVS patients use cannabis to relieve vomiting/abdominal pain during attacks (likely not CHS)
  • Overall prevalence: 0.12%; US populations: 0.4%
  • Cannabis use among CVS patients increased 10-fold (2005–2014)
  • 18% of CVS patients, 39% of cannabis-using CVS patients have CHS
  • More common in men; median diagnosis age: 28 years
  • >4 year diagnostic delay in 40% of patients
  • One review: 22% used cannabis >11 years, 17% for 6–10 years, 36% for 2–5 years
  • Cannabis use: ≥daily in 61%, weekly in 19%
  • Diagnoses doubled (2000–2015) → likely due to higher THC content products
11. Nausea and Vomiting Disorders: Pathophysiology
11.1 CNVS Pathophysiology
  • Multifactorial
  • Insular cortex, amygdala, putamen, pons, other cortical regions contribute to nausea perception
  • Dorsal vagal complex and vagal pathways regulate vomiting
  • Most studies: poor correlation of delayed GE to nausea/vomiting severity
  • One study: FD patients with normal GE had nearly identical symptoms to gastroparesis patients with delayed GE
  • GE labile: >1/3 of patients switched GE rate group at 48 weeks follow-up
  • Review restricting GE analyses to optimal methods: delayed GE correlated with nausea, vomiting, early satiety/fullness, abdominal pain (OR 1.5–2.94)
  • Histopathologic findings from full-thickness gastric specimens: poorly relate to GE; similar reductions in interstitial cell of Cajal populations in delayed vs normal GE
11.2 CVS Pathophysiology
  • Occurs in isolation or with GI, neurohumoral, autonomic, genetic factors
  • Rapid GE found in 40–80% of CVS patients between vomiting episodes
  • Delayed GE described in 27%
  • Autonomic abnormalities and sympathetic dysfunction prevalent
  • Personal/family histories of migraines often reported
  • CVS flares in some women begin before menstruation (catamenial CVS)
  • Some cases exhibit maternal inheritance → suggests mitochondrial DNA abnormalities
  • Associated genetic factors:
  • Polymorphisms of
11.2 CVS Pathophysiology (continued)
  • Polymorphisms of cannabinoid and μ-opioid receptor genes
  • Single-nucleotide mitochondrial DNA polymorphisms (16159T and 3010A)
  • Calcium channel gene type-2 ryanodine receptor mutations
  • Endocannabinoid-related lipids and salivary cortisol elevated during emetic episodes

Triggers of flares:

  • Psychological stress and catastrophizing
  • Physiological stressors: infection, altered food intake, exercise, impaired sleep
  • Food triggers: cheese, cured meats, chocolate, monosodium glutamate

Psychiatric comorbidity: 78% of adults with CVS screen positive for depression, 84% positive for anxiety

11.3 CHS Pathophysiology
  • Multifactorial mechanisms for symptom induction
  • THC contributes to both antiemetic and proemetic actions of cannabis
  • Postulated: CHS results from downregulation, desensitization, or internalization of CB1 receptors in HPA axis and sympathetic nervous system
  • Changes in TRPV1 receptor function also prominent
  • 59% of CHS patients screen positive for anxiety, 68% positive for depression
12. Nausea and Vomiting Disorders: Clinical Evaluation
12.1 CNVS Clinical Evaluation

Differential diagnosis includes:

  • Gastroparesis, mechanical obstruction, metabolic disorders, autoimmune disease, infiltrative disorders, psychiatric illnesses, intracranial masses, inner ear disease, medications
  • Role of chronic cannabis use as cause of CNVS: controversial

Diagnostic testing dictated by clinical presentation:

  • Bilious vomiting, abdominal tenderness, abnormal neurological findings, worsening vomiting → warrants evaluation
  • Blood work: excludes electrolyte abnormalities and metabolic disorders
  • Endoscopy or imaging: evaluates for organic disease
  • Specialized GI function tests: offered in selected settings
12.2 CVS Clinical Evaluation

Four phases characterized:

1. Prodrome: nausea, abdominal pain, fatigue, weakness → initial presentation, can be stereotypical in timing

2. Emetic phase: 3–6 days, unrelenting vomiting >8 times/hour on average → within minutes to hours after prodrome

  • Nearly 2/3 report abdominal pain and diarrhea during this phase

3. Recovery phase: up to 1 week → persistence of nausea, lightheadedness, meal intolerance in some patients

4. Interepisodic phase: weeks to months duration

Additional findings:

  • Up to 63% of CVS patients have milder nausea, dyspepsia, intermittent vomiting between attacks
  • Fluid loss, electrolyte abnormalities, hematemesis may occur acutely
  • Dental enamel damage with repeated attacks
  • Compulsive hot bathing behavior: 48% of CVS patients who do not use cannabis

Diagnostic testing: performed only to exclude other causes of chronic nausea/vomiting → negligible yield

12.3 CHS Clinical Evaluation

Four phases similar to CVS:

  • Acute emetic phases: few hours to 1 week, vomiting >20 times daily with abdominal pain, diarrhea, autonomic symptoms
  • One review: up to 18% of cases not characterized as episodic emesis → possibility that not all CHS cases mimic CVS

Compulsive bathing behaviors: 92% of patients report to reduce vomiting and pain during attacks

Factors associated with CHS diagnosis:

  • Cannabis use >1 year
  • Daily cannabis use, weekly cannabis use
  • Symptom resolution with cannabis abstinence
  • Compulsive bathing to relieve symptoms
  • Male sex, age <50 years

Diagnostic challenges: confirming symptom resolution after cannabis cessation → roadblock in many cases

  • Only 19% able to abstain from cannabis for >4 weeks
  • Cannabis metabolites persist >1 month; brain impairments may endure longer
  • Proposed: cannabis cessation >6 months or >3 typical CHS cycles for diagnosis

Testing: rarely indicated in absence of complications (e.g., hemorrhage)

  • Urine drug testing for THC metabolites: considered for patients who deny cannabis use
  • No metabolite profile specific for CHS
13. Nausea and Vomiting Disorders: Treatment
13.1 CNVS Treatment
  • Little investigation on CNVS treatment
  • Antiemetic agents: antagonists of H1, D2, 5-HT3, neurokinin (NK)1 receptors; agonists of cannabinoid CB1 receptors
  • Other therapies: TCA and psychological measures show benefits in some patients
  • Limited data supporting ginger, herbal remedies, electroacupuncture
13.2 CVS Treatment

Abortive treatment: may not be feasible if prodrome is short; non-oral treatments most likely beneficial after emesis starts

  • 5-HT3 antagonist ondansetron: commonly used for CVS attacks, but no trials specifically in CVS
  • NK1 antagonists (aprepitant, fosaprepitant): reduce emesis frequency and hospitalizations in refractory patients
  • Sedating agents: benzodiazepines, H1 antagonists → often beneficial adjuncts to antiemetics
  • Intranasal or injectable triptans: reduce vomiting and abdominal pain, especially with family migraine histories

Preventive treatment:

  • TCA: improvements in 69% of CVS patients
  • Poor responses in those with migraines, psychological illness, cannabis or opioid use
  • Topiramate (anticonvulsant): reduced attacks and healthcare utilization in 65% of patients
  • Patients refractory to TCA: 50% fewer CVS attacks on zonisamide or levetiracetam
  • Mitochondrial supplements (coenzyme Q10, L-carnitine, riboflavin): some prophylactic efficacy
  • Psychological therapy: CBT advocated for some patients
  • Integrative health care model (mediation + care coordination): superior outcomes
13.3 CHS Treatment
  • Several reports confirm cannabis cessation leads to CHS resolution
  • Resuming cannabis use promotes symptom resurgence
  • CBT: may help reduce cannabis dependence in CHS

Abortive therapies:

  • Cutaneous capsaicin (TRPV1 agonist): shortens CHS episodes, decreases therapy requirements
  • Hot showers: activate skin TRPV1 thermoreceptors → plausible mechanism for benefit
  • Parenteral D2 antagonists haloperidol and droperidol: efficacy in aborting CHS episodes (uncontrolled series + controlled trial)
  • Benzodiazepines (lorazepam, alprazolam): relief in small series

Preventive therapy: CHS responds poorly to TCA

  • One small series: effective prophylaxis with olanzapine
14. Excessive Belching Disorders: Definition and Epidemiology
14.1 Definition
  • Belching (eructation, ructus): audible escape of gaseous material from esophagus or stomach into pharynx
  • Two distinct types: gastric belch and supragastric belch
  • Disorder only when excessive and bothersome (applies to both types)
14.2 Epidemiology
  • RFGES: overall prevalence of Rome IV belching disorders = 1%
  • Referred patients with upper GI symptoms: prevalence several times higher
15. Excessive Belching Disorders: Diagnostic Criteria (B3)
  • Bothersome belching from esophagus or stomach >3 days/week
15.1 Subcategories
  • B3a: Supragastric Belching (from esophagus)
  • B3b: Gastric Belching (from stomach)
15.2 Supportive Criteria

1. Supragastric belching strongly supported by observing frequent, repetitive belching

2. Supragastric belching can be interrupted by maneuvers or distraction

3. Excessive gastric belching: no defining clinical correlate

4. Intraluminal esophageal impedance measurement (with or without manometry): allows objective differentiation of supragastric vs gastric belches

  • Criteria: last 3 months, onset ≥6 months prior to diagnosis
16. Excessive Belching Disorders: Pathophysiology
16.1 Gastric Belching
  • Physiological reflex triggered by distension of proximal stomach
  • Results in transient relaxation of lower esophageal sphincter (TLESR)
  • Rapid distension of esophagus by large volume of gas → relaxation of upper esophageal sphincter (UES)
  • Gaseous distension caused by: air swallowing, ingestion of carbon dioxide source, mechanical inflation (respirator, sleep apnea equipment)
16.2 Supragastric Belching
  • Eructated air does not originate from stomach → either sucked or (less commonly) injected into esophagus from pharynx, then expelled immediately
  • Not accompanied by TLESR
  • Occasional supragastric belching: occurs in most healthy subjects
  • Patients with excessive supragastric belching: more belching events but do not swallow more air than gastric belchers
16.3 Impact on Quality of Life
  • Patients with excessive supragastric belching: significantly impaired health-related QoL → primarily social function and vitality impairments
  • High prevalence of anxiety disorders
  • Symptoms aggravated during stressful events
  • Distraction reduces belching frequency; drawing attention increases frequency
16.4 Relationship with GERD
  • Belching: one of most frequently reported symptoms in GERD patients (after heartburn and regurgitation)
  • Partially explained by higher incidence of air swallows and higher frequency of gastric belching
  • Study comparing Rome IV excessive belching patients with GERD patients: most common type in both groups was supragastric (93% vs 87%)
  • Several groups described temporal relationship between supragastric belches and reflux events → subject's response to unpleasant sensation
  • Incidence of these belches diminished by acid suppressive treatment
  • Opposite sequence (supragastric belch first, reflux second) also found more often than expected
  • Hypothesis: supragastric belches can provoke reflux in subset of patients
  • Supported by observation: treatment of supragastric belching with CBT reduces acid reflux
17. Excessive Belching Disorders: Clinical Evaluation
  • Patients presenting with excessive belching: more likely supragastric than gastric, especially when frequency very high (e.g., 10–